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Activation of STAT3/5 signal pathways in complete mole and repression in choriocarcinoma cell lines

Hidenori Kato1, Takafumi Inoue, Kazuo Asanoma

  • 1Division of Molecular and Cell Therapeutics, Department of Molecular Genetics, Medical Institute of Bioregulation, Kyushu University, Tsurumihara 4546, Beppu City, Oita 874-0838, Japan. hidekato@beppu.kyushu-u.ac.jp

The Journal of Reproductive Medicine
|February 18, 2006
PubMed
Abstract

Insights

Signal transducer and activator of transcription (STAT) signaling and survivin are upregulated in complete mole (CM). However, choriocarcinoma (CC) cells maintain survivin expression via MEK signaling, independent of STAT activation.

Area of Science:

  • Molecular biology
  • Signal transduction pathways
  • Trophoblastic diseases

Background:

  • Previous microarray studies suggested STAT5 and survivin upregulation in complete mole (CM).
  • The role of STAT-mediated signal transduction in CM and choriocarcinoma (CC) requires clarification.

Purpose of the Study:

  • To investigate the status of STAT-mediated signal transduction in CM and CC.
  • To determine the role of STAT and MEK signaling pathways in survivin expression in these conditions.

Main Methods:

  • Western blot (WB) analysis of STAT3 and STAT5 activation in CM, normal villi, and CC cell lines.
  • Inhibition of STAT and MEK pathways to assess changes in survivin expression.
  • Immunohistochemical staining of CM and normal villi for pSTATs.

Main Results:

  • Phosphorylated STAT3 and 5 (active forms) and survivin were significantly upregulated in CM compared to normal villi.
  • Immunohistochemistry revealed pSTAT signals in CM trophoblast layers, absent in normal villi.
  • CC cells showed minimal pSTAT detection by WB but maintained high survivin expression via MEK pathway activation.

Conclusions:

  • Activated STAT signaling likely contributes to the hyperplastic growth of trophoblasts in CM.
  • CC cells may achieve tumor growth independently of cytokine-driven STAT signals during carcinogenesis.
  • MEK pathway activation is crucial for survivin expression in CC, suggesting alternative oncogenic mechanisms.

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